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Thursday, February 12, 2015

What's a 'healthy diet' anyway?

A nutrition advisory panel is convened by the US Department of Agriculture every five years to review recent research in the field, make sense of it, and offer recommendations about what Americans should be eating for optimal health. Those food pyramids, MyPlate, decades of advice to limit our cholesterol, saturated fat and salt intake? All the work of these panels of experts who scoured the data and told us what it meant. And as a result, from the 1960's onward, good, conscientious people reduced their cholesterol intake, took the salt shaker off the table and the whole milk and butter out of the refrigerator, cattle were bred to be leaner, eggs were banned from breakfast, low-salt and low-fat processed foods appeared on the shelves, and heart disease death rates ... continued to fall.

Now, according to numerous news accounts, including here at the Washington Post, after more than 50 years of anti-cholesterol, anti-fat expert advice, the current advisory panel is reportedly poised to recommend that we need no longer need to limit the amount of cholesterol we eat, nor worry about our salt intake. Bring on the shrimp, the lobster, the eggs, the meat, banish the guilt!

Oh, wait. Hold on a sec. Let's go back to those falling heart disease rates. I remember one of the first lectures I heard as a new grad student at the University of Texas School of Public Health in the late 1970s, given by heart disease epidemiologist Reuel Stallones, Dean of the school. His point was that rates had been falling since the 1960's and epidemiologists had no idea why. He systematically destroyed every argument then (and now) current that might explain the rise and fall of heart disease death rates -- changing diet, decreased smoking, de/increased exercise.

In fact, he made the same case in 1980 in Scientific American in an article called "The Rise and Fall of Ischemic Heart Disease". (The terms ischemic heart disease, coronary heart disease, and arteriosclerotic heart disease are more or less interchangeable, according to Stallones.)

In the U.S. the death rates attributed to heart attack and other results of the obstruction of the arteries that nourish the heart have fallen since the 1960's. Why they have is not understood.

Here's Stallones' graph of heart disease death rates, from 1900 to 1980. I can't explain why deaths are still rising in the above graph in the 1950's, but falling in this graph; presumably this has to do with differing classifications of deaths due to heart disease. Anyway, here rates rose rapidly starting in 1920 and then began to fall in the 1950's, steeply in the 1960's.

Here's another graph showing the decline more or less in line with Stallones' data, from a 2000 paper in Circulation.

"Death rates for major cardiovascular diseases in the United States from 1900 to 1997. *Rates are age-adjusted to 2000 standard." Source: Circulation, Cooper et al., 2000

As Stallones wrote, "Plainly a sustained decline in the death rate for ischemic heart disease commands attention and calls for explanation." And, he backs up to ask not only why the fall, but why it was that heart disease mortality began to rise so quickly in 1920, particularly among men. Whatever explains the decrease must also explain the increase.

Smoking began to rise after World War 1, which fits the rise in heart disease mortality, and began to decrease from the mid-1960's or so, which fits the decrease. But such an explanation would assume no latency period between beginning to smoke and its effects on heart disease. And, middle-aged men quit smoking at higher rates than women, and this is not, as Stallones said, in concordance with the pattern of decline in heart disease mortality. Treatment isn't an effective explanation either, because incidence rates -- new cases -- followed the same pattern as mortality.

He concluded,

In summary, four major variables are known to be associated with the risk of ischemic heart disease in individuals. Among the four, hypertension does not fit the trend of the mortality from ische­mic heart disease at all; physical activity fits only the rising curve, serum choles­terol fits only the falling curve and only cigarette smoking fits both. In no case is the fit as precise as one would like. This raises doubt that any of the factors is a fully satisfactory explanation for the variation in mortality.

So, in sum, as of 1980 epidemiology had no explanation for the rise and fall of heart disease mortality rates.

And epidemiology still can't tell us what causes heart disease, or predict who'll get it. So, apparently we'll soon be told that we no longer have to monitor our cholesterol intake, and there's a lot of talk about fat consumption not being linked with heart disease anymore, and it's not clear whether obesity or hypertension are actually causal. At least smoking is probably still a problem.

It's clear from the rise and fall of death rates through the 20th century that genes aren't going to be the major explanation because genes can't explain the spike in the 1920's and the fall 40 years later. That experience also makes it clear that we can't predict environmental changes (or, often, even figure out what they were in hindsight) that might be associated with risk, and thus we aren't going to be able to predict the future, despite the claims of precision medicine advocates.

Stallones suggested that heart disease mortality data might indicate a single environmental cause to explain the rise and fall of death rates, but found reasons to argue against each of the most obvious ones. Could the cause have been inflammatory? If so, that would reinforce the idea that predicting future environments and causes is not going to be possible.

And, if there was a single cause, it's curious that our reductionist approaches, with large carefully designed samples and sophisticated statistical analysis, were unable to identify it, because that's what they are widely thought to be best at. This makes it more likely that heart disease in populations has multiple causes. And in fact every heart attack is unique, because no two people eat the same things, do the same amount of exercise, suffer the same infectious diseases, and so on. So maybe the very word 'cause', and the very approach (statistical), both of which assume some regular, replicability properties, are not being appropriately conceived. This is a subject we'll discuss next time.....

"Experts" responding to the coming cholesterol recommendations have said that we still need to eat a healthy diet. But when we still have no idea what's unhealthy, it's hard to know what is.

2 comments:

David J. Littleboy
said...

My understanding on cholesterol is that the relationship between cholesterol in the blood and heart disease is well established, and remains seen as medically significant. What has changed is that it's been found that cholesterol intake and blood cholesterol levels are _NOT_ necessarily related. (I think this was discussed over at the Incidental Economist.) So we can eat eggs again.

But this all assumes a diet whose total calories don't exceed your calories consumed.

Still, the point that heart disease is decreasing and there's no obvious reason why is fascinating.

Well, in fact, even the cholesterol/heart disease link has been questioned. I know we've written about it before, and searching on 'cholesterol' pulled up a bunch of posts, but here's just this comment in Nature from 2013.

Indeed, even the long-held idea that energy imbalance is what causes obesity is being questioned. I admit to raising my eyebrows at this, but that's largely based on belief, not evidence.

There are several lessons here. One, epidemiological methods aren't quite up to the problems of complex diseases. And, everything in moderation.

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